Schizophrenia

“A Slow Fire Burning”

Dr C Christie

General

Schizophrenia is a major psychotic disorder Chronic debilitating illness Devastating effects on all aspects of patient’s life Comprehensive and continuous lifelong treatment Heterogeneous disorder Variation in presentation Clinical diagnosis No single symptom pathognomonic of 295

3 Symptom clusters

Positive symptoms – hallucinations and delusions

Disorganised thought, behaviour and speech

Negative symptomsAffective flattening, alogia, anhedonia and

avolition

History

Kraeplin (1856 – 1926) termed dementia precox (early onset of cognitive decline)

Bleuler (1857 – 1939) used term schizophrenia.

Schism between thought, emotion and behaviour

Does NOT mean split personality

DSM IV

A. Characteristic symptoms (2 or more)Delusions, hallucinations, disorganised speech

Grossly disorganised or catatonic behaviour

Negative symptoms

B. Social/occupational dysfunction

C. Duration: 6 months

D. Exclude schizoaffective and mood disorder

E. Exclude GMC and substances

F. Exclude pervasive developmental disorder (autism)

Subtypes

Disorganised Paranoid Catatonic Undifferentiated Residual

Epidemiology

1% prevalenceRisk increased if first degree relatives

have the disorderRisk increased if person is single,

industrialised nation, in lower SE class, urban, problems in utero, perinatal problems, born in winter, recent stressful life event

Age and Sex. M = F

Males

Present at earlier age

Peak in early 20’s

Poorer premorbid personality and social adjustment

Females

Peaks in late 20’s and 30’s

Better prognosis

Fewer admissions, shorter length of stay

Mortality and morbidity

Mortality twice that of general populationSuicide high, 50% attempt10 -15% successfulHigher risk of dying a violent deathGMC present needs to be vigorously

diagnosed and treated

Substance Abuse

Co-morbidity of substance abuse and schizophrenia very common

30 – 50% alcohol abuse15 – 25% cannabisNicotine!

Genetics

Sibling of schiz patient 8%Dizygotic twin 12%Child of one schiz parent 12%Both parents with schiz 40%Monozygotic twin 47%

Cultural and socioeconomic

Found in all cultures and socio-economic groups

In developing countries prognosis and outcome better

Related to stronger family/social supportHomelessness and 295 linkedDownward drift and deinstitutionalisation

Biological factors/ structural

Changes in limbic system, basal ganglia and frontal cortex

Enlarged lateral and third ventriclesReduction in cortical volumeCytoarchitextural abnormalities of

amygdala,hippocampus and parahippocampal gyrus

Neuroimaging

Abnormal PET scans,shows deranged glucose utilisation/cerebral blood flow when challenged with psychological task, hypoactivity of frontal lobes and intellectual testing may show deficits

Is 295 a neurodevelopmental disorder only manifesting later in life with microanatomical cortical dysgenesis?

Neurochemistry

Neurochemical abnormalities central Models have been hypothesised using drug

induced psychotic models Dopamine hypothesis: hyperdopaminergia is

main protagonist Drugs that reduce firing of mesolimbic

dopamine neurons have antipsychotic effect Drugs that stimulate dopamine increase

psychosis

Neurochemistry

Hypothesis revised Low prefrontal dopamine causes deficit,

negative symptomsExcessive dopamine activity in

mesolimbic dopamine neurons cause positive symptoms

Dopamine AND serotonin

Atypical neuroleptics act as 5HT2 and

Dopamine antagonists5HT2a, 5HT2c antagonism, 5HT1a

agonismCholinergic, muscarinic, GABA and

glutamate mediated actions modulate antipsychotic drug action

Clinical features/Acute phase

Behaviour and appearance – normal, perplexed, sudden behavioural changes

Speech – vague, concrete, bizarre, pressure, poverty, word salad, neologisms

Range of affect – blunted Auditary hallucinations common Voices often derogatory and refer to patient in

3rd person Delusions Insight is reduced

Chronic Phase

Psychotic symptoms may be less severeSymptoms persist in attenuated formNegative symptoms may predominate

Delirium Schizophreniform

disorder Schizoaffective

disorder Delusional disorder Brief psychotic

disorder

Bipolar mood disorder

Substance induced psychotic disorder

Psychosis secondary to GMC – TLE, epilepsy

Course and prognosis

10 -15% have a good prognosis20 – 30% lead reasonably normal lives40 – 60% poor outcome with chronic

deteriorating courseParanoid subtype best prognosisDisorganised subtype worst prognosis

Course and prognosis

Symptoms begin in adolescenceMay have prodrome diagnosed in

retrospectEach relapse followed by deteriorationPositive symptoms may become less

severe over timePsychosis is toxic for the brain!

Good prognostic indicators

Later onset Female gender Absent family hx Marriage Good pre-morbid

personality and psychosocial adjustment

Obvious precipitant Positive symptoms Good support

systems Mood symptoms with

family history of mood disorder

Management

Involve family and patient in active collaboration using integrated approach with pharmacologic, psychotherapeutic, psychosocial and rehabilitative measures

Need comprehensive and continuous treatment

At present NO CURE

General goals of treatment

Decrease frequency, severity and psychosocial consequences of episodes

Maximise psychosocial functioningEstablish and maintain therapeutic

allianceMonitor patient status at regular intervals

Thorough initial workup

Rule out conditions that mimic 295Identify co-morbid conditions that

complicate diagnosis and treatmentEstablish baseline for monitoring course

of illness and response to treatment

Acute phase management

HOSPITALISE IF:o Poses a threat to self or otherso Unable to care for selfo Co-morbidityo First episodeo Substance abuse o May need involuntary hospitalisation

Antipsychotics

Biological treatment the mainstay Typical antipsychotics – high potency –

haloperidol, low potency – chorpromazine Atypical antipsychotics – clozapine,

respiridone, olanzipine, quetiapine. Useful for negative symptoms, poor responders and patients prone to side effects

Choice of drug depends on age, physical status, co-existing medical problems

Drug treatment

60% of patients on antipsychotics for 6 weeks improve

If meds of well patient stopped 75% relapse in 6 – 24 months

First episode patients – 40 – 60% relapse during the year after episode if not on medication

Duration of treatment - debate

First episode: 1 – 2 years of maintenance

Multiple episodes: minimum of 5 yearsViolent or aggressive behaviour or

suicide attempts need indefinite treatment

Psychosocial treatment

Become ill during critical career forming years

Psychosocial interventions need to be integrated with psychopharmacological treatments

Focus on improving social functioning in the hospital, community, at home and at work

Rehabilitation

Programmes emphasise social skills training and vocational training

NB for community based treatmentCognitive remediation can assist

recognition and treatment of cognitive impairments

Distractibility, memory problems, lack of vigilance, limitations in planning and decision making

Individual psychotherapy

Supportive, reality orientated individual therapy

Individual and groupsTeach coping and problem solving skillsPsychotherapy is not a substitute for

medication and is helpful once antipsychotics have started working

Families

Grief with no end Teach family to recognise early signs of

relapse Psycho education to help families deal with

disease profile Blame should not be placed on patient for

pathology Families who are highly critical or

overprotective can increase relapse

Families

Group therapy enhances problem solving, goal planning, social interactions

and medication and side effect management

A lot more could be done for schizophrenics in our society!

References

Kaplan and Sadock’s Synopsis of Psychiatry eighth edition. pp 456 - 491 APA guidelines. Practice guideline for the

treatment of patients with Schizophrenia. Am Jnl Psychiatry 154: 4 April 1997 (supplement)

Carpenter WT, Buchanan RW. Schizophrenia. New England journal of Medicine. Vol 80, March 1983

Schizophrenia focus. The Lancet. Vol 346. Sept 9, 1995.